http://dx.doi.org/10.1590/S0034-70942002000300012

BACKGROUND AND OBJECTIVES: Smoking is
becoming very important for anesthetic morbidity. In spite of its widespread
noxious effects on health, developing countries have increasing statistics on
smoking population. This review aimed at showing action mechanisms and effects
of cigarettes on different organs and systems, and their impact on physiology,
preoperative risk and management of smokers during preanesthetic preparation,
in addition to postoperative complications.CONTENTS: Several action mechanisms of cigarettes and their components
on organ and systems, organic consequences and the anesthetic approach to decrease
perioperative morbidity in those patients are presented.CONCLUSIONS: Smoking history in preanesthetic evaluation should be highly
valued and preventive measures should be taken with regard to systemic effects,
thus minimizing surgical and anesthetic risks.

Smoking is becoming very important for anesthetic
morbidity. In spite of its widespread noxious effects on health, developing
countries have increasing statistics on smoking population. Postoperative pulmonary
complications are 2 to 6 times more frequent in smokers as compared to nonsmokers.
Smokers have a 70% higher risk for cancer, cardiovascular or pulmonary disease,
as compared to nonsmokers 1. In industrialized countries, approximately
1/3 of the adult population smoke and around 20% of natural deaths are attributed
to tobacco consumption 2,3. In Brazil, 80 to 100 thousand people
die every year from smoking-related diseases 4; in the world, approximately
3.7 million people die, being 1/3 in developing countries. This study aimed
at reviewing cigarettes action and effects on several organs and systems, considering
their impact on physiology, preoperative risk and management of smokers during
preanesthetic preparation, in addition to postoperative complications.

PHARMACOLOGY

Nicotine is known by men since 1828 and was isolated
by Posselt and Reiman; posteriorly, its pharmacology was studied by Orfila in
1843 5. Several organs and systems are damaged by the continuous
use of tobacco, which has more than 4000 substances in the smoke, some of them
with active pharmacological cytotoxic, antigenic and mutagenic action, including
at least 43 carcinogens, and are responsible for a wide range of noxious effects
1,6. Most affected organs and systems are heart, GI tract, lungs,
blood and immune and nervous systems. Special attention must be given to the
respiratory system which directly receives inhaled gases. One may also mention
effects on homeostasis, drug metabolism and patients psychism. Undoubtedly,
nicotine is today the most widespread dependence-producing substance 7.

From the total smoke produced by a cigarette,
approximately 92% to 95% are in the gaseous phase; from these, 85% are nitrogen,
oxygen and carbon dioxide; the remaining gases, presented as non-condensed vapors
and material particles determine most clinical manifestations of medical importance.
Some compounds of those gases act directly on mouth, nose, pharynx and tracheobronchic
tree mucosa, while others are absorbed by the blood or dissolved in the saliva
and swallowed 1.

NICOTINE PHARMACOLOGICAL PARTICULARITIES

Nicotine is an alkaloid with dose-dependent ganglionary
stimulating and depressing action. Smokers have, in general, 15 to 50 ng.ml-1
nicotine levels. This substance acts on different areas: carotid body and aorta
chemoreceptors, in autonomic ganglia through catecholamine release by the adrenal
medulla and other chromaffin tissues. Major acute effects include increase in
systolic and diastolic blood pressure, heart rate, inotropism and peripheral
vasoconstriction. Direct nicotine vasoconstriction may increase coronary vascular
resistance impairing blood flow, especially in patients with stenotic coronary
lesions. All those effects result in an unfavorable environment for myocardial
oxygenation in terms of supply/demand ratio. There is an increase in norepinephrine,
epinephrine, growth hormone, cortisol and vasopressin plasma levels 1,8.

Nicotine is absorbed by the skin, mucosa (stomach
and intestines) and lungs, being transported by blood flow, reaching the central
nervous system (CNS) and acting in approximately 7 seconds by the release of
endogen opioids and glucocorticoids 5,7.

It is metabolized by liver (80% to 90%), lung
and kidneys (in a lower ratio). Nicotine and its major metabolites - cotinine
and nicotine-n-oxide - are promptly excreted by the kidneys, especially in acidified
urine. Nicotine plasma half-life after inhalation is 30 to 60 minutes. Although
being highly toxic, nicotine is eliminated after one night abstinence. After
this period, there is a decrease in heart rate, blood pressure and catecholamine
levels. After preanesthetic medication administered at night, patients should
be advised not to smoke before sleeping. Cotinine may be measured in urine,
blood and saliva and is largely used as a smoking habit determinant 6;
since it has a long elimination half-life (more than 20 hours), it may be used
to evaluate patients adherence to preoperative abstinence recommendations.
Cigarettes themselves represent 8 to 9 mg of nicotine and only 1 mg is systemically
made available to smokers because smoked tobacco has 1% to 2% nicotine 5.

Carbon monoxide (CO) is a toxic gas interfering
with oxygen transportation and utilization. It is important to remind that hemoglobin
(Hb) affinity for CO is approximately 200 times higher than for oxygen; even
in low CO alveolar concentrations, smokers have significant amounts of carboxyhemoglobin
(COHb) (5-15% in smokers; 0.5 to 3% in nonsmokers), due to Hb metabolism and
air pollution 1. CO is only excreted by breathing and has a rather
stable binding to Hb, which may be detected even after death 9.

Cigarette smoke inhalation increases pulmonary
microvascular patency with the production of free radicals allowing the assumption
that these substances may be important in the pathogenesis of tobacco-induced
diseases such as emphysema 10.

Among major carcinogens, one may mention polinuclear
aromatic hydrocarbons, aromatic amines and nitrosamines. Some mutagenicity indicators
are increased in smokers lymphocytes as compared to nonsmokers. Carcinogenesis-related
substances, such as catechol, phenol and cresol groups are also found in the
smoke 1.

Nicotine is classified as an insecticide with
potential toxicity. Clinical symptoms are salivation and vomiting, followed
by muscle weakness and prostration, with blood pressure decrease and weak pulse
and culminating with chlonic seizures and respiratory arrest 9. There
may also be visual or auditory changes, abdominal pain, mental confusion and
cold sweating. It is estimated that 60 mg is the nicotine dose needed to cause
death. Intoxication treatment includes, gastric lavage, ipecac emetic syrup,
in addition to support therapy for hemodynamic and respiratory changes 5.

TOBACCO ACTIONS ON DIFFERENT ORGANS AND SYSTEMS

Cardiovascular System

There is a cardiovascular system theft
since there is a higher oxygen consumption through the sympathetic-adrenergic
system activation. At the same time, there is an oxygen supply decrease by increased
COHb levels and coronary vascular resistance increase. Smoking is the major
risk factor for arterial thromboembolism and coronary vasospasm through multiple
ways, including direct endothelial and hematological damage and metabolic and
biochemical abnormalities 3,6. This substance may increase and even
decrease heart rate by acting on sympathetic and parasympathetic systems, in
addition to aortic and carotid chemoreceptors 5.

Clinical correlations have not been shown for
all those pathophysiological events in terms of anesthesia. Especially, an increase
in acute myocardial infarction and unstable angina has not been significantly
observed in smokers, in spite of severe cardiovascular physiological changes.
Short abstinence periods may influence results due to the relatively short nicotine
(30 to 60 minutes) and COHb (4 hours) elimination half-life.

Nicotine action has a two-phase pattern on autonomic
ganglia and adrenal medulla, with an initial stimulating effect in low doses
and posterior stimulation decrease with higher doses. Increased nicotine concentration
causes hypotension and neuromuscular flaccidity because the drug has a ganglionic
blocking effect 16. The association of its sympatheticomimetic effects
may produce coronary vasospasm and cardiac arrhythmias, even when the patient
is a user of slow release nicotine patches, as observed by Williams and Tempelhoff
5,11. These effects contribute to increase cardiovascular morbidity,
associated to coronary vasoconstriction and increased myocardial O2
consumption.

Respiratory System

Respiratory system changes include mucous hypersecretion
and tracheobronchic tree damage by long-term obstruction, as well as restriction
of small airways with increased closing ability and trend to changes in the
perfusion-ventilation rate. There is also an increase in reflex sensitivity
of both conduction ways (high and low), in respiratory epithelium patency and
evidences of surfactant factor loss. Further events with anesthetic implications
are cell-mediated humoral immunity impairment, in addition to microsomal enzymes
induction with the increase in several drugs metabolism 6.

Inveterate smokers have COHb levels of 5% to
15%, which may mean oxygen saturation below 15% indicated by pulse oximetry
(oxygen combined to Hb / oxygen transportation ability X 100). In practice,
available oxygen would be even lower since COHb shifts Hb dissociation curve
to the left. Inherent damage could be measured through increased sympathetic
activity and airway hyper-reflex 3,6,12,13.

Hb saturation decrease and hypoxemia (SaO2
< 84%) should also be considered both in inveterate smokers and youngsters.
This hypoxemia is often attributed to an increase in closing volume and decreased
functional residual capacity. So, O2 should always be offered to
those patients during PACU transfer and stay where pulse oximetry is mandatory
1.

With age, excitation threshold tends to be naturally
increased due to a decrease in nervous terminations which, combined with upper
airway mucosa thickening, decreases the penetration of noxious chemical agents
and increases aspiration risk 13. This finding justifies more attention
during anesthesia or sedation recovery of geriatric patients.

Major smoking-induced enzymatic changes are concentrated
on system P-448. There is no action on liver blood flow. In spite of thiocyanate,
substance produced by tobacco smoke, be increased in serum levels of smokers,
this is not an indicator of plasma nicotine, cotinine and COHb importance 1.

Approximately ¼ of smokers have chronic
bronchitis, which is five times lower in nonsmokers 2. There are
evidences that smokers are more vulnerable to upper airway problems, including
laryngospasm during anesthetic sedation and emergence. Indirect evidences show
that the same problems are reflected in lower airways. However, a clearer demonstration
of increased morbidity has been related to preoperative lung complications,
such as atelectasy and pneumonia, which are two to six times more frequent in
smokers 1,6,12,13.

The obstruction by thich mucus in the bronchioli
is frequent in pulmonary inflammatory processes, such as asthma and chronic
obstructive disease, and sometimes it can be found in larger bronchi 14.
Chronic bronchitis and emphysema may determine pulmonary hypotension with right
ventricular failure. Chronic smoking decreases ciliary transportation and cough
is a major factor to remove tracheobronchic secretions. Many cigarette components
(hydrocyanic acid, acetaldehyde, acrolein, formadehyde, nitrogen oxides) are
ciliostatic and ciliotoxic. Smoking abstinence decreases sputum in 50% if lasting
for more than 6 weeks and with time, ciliary activity returns to normal 1.

Irritating receptors of fast adaptation are found
in all airway cartilaginous structures, being more abundant in the trachea and
especially the carina. These receptors respond to mechanical or thermal irritation,
inhaled particles or gases. Airway edema and histamine release also activate
them, resulting in cough reflex, bronchoconstriction and mucus secretion. Conversely,
juxtapulmonary receptors are adjacent to pulmonary capillary located in alveoli
interstitium. These seem to respond to pulmonary congestion, edema, inflammation
and vigorous exercise. They have a major role in the sensation of dyspnea following
situations such as pulmonary congestion 18.

All inhaled CO is excreted without changes by
the lungs. A major factor for CO excretion is increased pulmonary ventilation
(decreasing PACO) and inspired O2 partial pressure 1.

Nitric oxide (NO) bronchodilating properties
are well-known. However Hill et al. 25 have evaluated patients with
different abstinence periods submitted to cardiac surgeries and have observed
that smokers had more nitric oxide synthetase activity, which is an enzyme precursor
to NO during cardiopulmonary bypass, and this would explain the increase in
pulmonary complications in this population as compared to nonsmokers.

Passive smokers have increased COHb levels as
well as more airway reactivity. Warner et al., in a study evaluating the incidence
of pulmonary complications after tobacco abstinence, have observed that there
was a higher risk for smokers stopping smoking for up to 8 weeks as compared
to those continuing smoking or nonsmokers. Beyond this time, the risk was similar
to nonsmokers. Pulmonary functionality abnormalities and the presence of secretions
could have caused this effect 1.

Long-term smokers (more than 30 years) often
have more signs and symptoms of pulmonary function deterioration and prominent
signs, such as sputum production. However, in shorter-term smokers and without
major symptoms, the possibility of reactive airways should also be considered
18.

GI Tract

Smoking effects on this system are mainly due
to a parasympathetic action with increased tone and intestinal motor activity.
Some studies have shown a delay in stomach emptying and an increase in baseline
gastric acidity in smokers, but such findings have not been confirmed by more
recent studies (Chart I)
5,6. Other studies have suggested that smokers could benefit from
the use of antacids or H2 receptors antagonist 1.

Renal System

Smoking is associated to antidiuretic hormone
release (ADH) with water retention and dilution hyponatremia, especially if
water ingestion is associated, leading to increased blood volume 1.

Gynecological System and Gestation

The increased risk for myocardial infarction,
subarachnoid hemorrhage and peripheral vascular diseases when smoking is associated
to contraceptives is well known 15. There would be a decrease in
high density proteins and an increase in low density proteins, favoring vascular
changes through a synergy between contraceptives and smoking.

A two-fold increase in risk for cervical neoplasia
is also reported in smoking patients as compared to non-smoking 15.

Schwilk et al. have found a male:female ratio
in the incidence of respiratory complications among young adults of 1:1.9 for
nonsmokers and 1:1.1 for smokers, indicating that young women would possibly
loose this advantage in becoming smokers 2.

Women who smoke during pregnancy have an increased
risk for spontaneous abortion, fetal death, neonatal death and sudden fetal
death syndrome. Smoking is also related to impaired conception and decreased
birth weight (in average 170 g) producing a condition known as tobacco fetal
syndrome. For mothers not smoking for 48 hours, there is an increase in available
O2 through a decrease in COHb levels, thus benefiting the neonate
during birth, especially during labor or when general anesthesia is induced
and, moreover, in the presence of maternal anemia 1. Nicotine can
also be detected in smoking womens milk.

Hematological System

There are known effects of CO over Hb and myoglobin,
shifting Hb dissociation curve to the left, in addition to P50, with
decreased O2 tissue supply. Smokers with normal O2 values
may present with reversible polycythemia, situation attributed to high COHb
concentrations 1.

Nervous System

Nicotine is a CSN stimulator. Low doses may cause
minor shiverings; as doses are increased, seizures may be present, ending in
CNS depression and death by respiratory failure, both by central paralysis and
respiratory muscles peripheral blockade. Action on the bulb may also cause emesis
and vomiting 5.

Pediatrics

Studies have shown in passive smoking children
an increased incidence of respiratory difficulties, such as asthma. Pulmonary
functions tend to be abnormal and there is an increased incidence in respiratory
tract infections. Evidences from ENT clinics indicate that living with smoking
parents determines a higher incidence of tonsillectomies in children 23.

Children with upper respiratory tract infections
are more susceptible to adverse effects during anesthesia due to the increase
in upper airway reflexes 3,12,23. During general anesthesia, pulmonary
gas exchanges are primarily deteriorated by functional residual capacity decrease,
resulting in airway closing. Infants and small children are more susceptible
than adults to functional residual capacity decrease and airway closing under
general anesthesia. So, they may develop postoperative hypoxia. In a study by
Motoyama and Glazener, 43 out of 97 patients had 91% or less oxygen saturation
(SaO2) in the immediate postoperative period, while Pulleritis et
al. have found 28.1% of children with less than 90% saturation during transfer
to PACU 23.

Smokers have more postoperative hypoxemia than
nonsmokers after similar anesthesia and surgery. There is an increase in airway
resistance and higher closing ability. There may be closing capacity during
anesthesia close to or beyond functional residual capacity, resulting in inadequate
ventilation/perfusion ratio, increased oxygen alveolar-arterial difference and
hypoxemia. These pulmonary function changes continue in the postoperative period
and may explain the higher hypoxemia level observed in smokers. Passive smoking
children have abnormal airway responsiveness and pulmonary function tests. It
is possible that the higher incidence of postoperative hypoxemia in those children
has a mechanism similar to that observed in smoking adults. Children do not
seem to respond to post-anesthetic hypoxemia through increased alveolar ventilation,
probably due to depressive anesthetics residual effects on carotid chemoreceptors.
So, oxygen supplementation is recommended for all children in the recovery room,
especially those with smoking parents 23.

There are evidences that 80% to 90% of smoking
adults start smoking during childhood or adolescence 6. In Brazil,
most parents smoke in the presence of their children and is frequent the worsening
of respiratory problems during weekends, when the contact with parents is more
intense. Respiratory problems frequency and intensity in small passive smokers
are directly related to the intensity of smoking at home 4.

PHARMACOKINETIC INTERACTION WITH OTHER
DRUGS

Several studies have shown the influence of cigarettes
on the pharmacokinetics of several drugs. Cigarette smoke has been indicated
as the cause of metabolism induction by enzymes, changing the half-life of drugs
processed in the liver, such as local anesthetics. Animal studies have concluded
that nicotine is enzyme-inducer. There is an acceleration of several substances
metabolism, such as ethylmorphine, norcodeine, aniline, benzopirene, indomethacin,
morphine, warfarin and bupivacaine, regardless of the route or the dose 19,22
(Chart II). It has been
suggested that the acute exposure to cigarette smoke would decrease indomethacin
plasma concentration due to the impaired GI tract absorption (since plasma concentrations
were not influenced by smoke when intravenously or rectally administered). This
may indicate a possible liver microssomal enzymatic induction during the first
days of cigarette exposure 22. A 6 to 8-week abstinence is suggested
to eliminate all metabolic changes of several drugs 1.

It seems to be a correlation between the number
of cigarettes smoked during the day and the effects on drugs. Some findings
are associated to tobacco consumption, such as metabolic acceleration (with
drug half-life decrease), increase in excretion and possible addition of drug
toxic effects 15.

Several drugs require higher doses in smokers
than in nonsmokers for adequate therapeutic effects. In spite of cigarette abstinence,
effects decrease may last for months, as it is the case with teophylline 15.
In other circumstances the interference may be indirect, such as peripheral
vasoconstriction, impairing muscle insulin absorption.

Some drugs may be changed by enzymatic induction,
such as some opioids and benzodiazepinics 6. Smokers under benzodiazepinics
seem to be more resistant to sedative effects than nonsmokers 19.

Tobacco does not act in an isolated manner to
change drug pharmacokinetics. Other factors, such as occupational diseases,
physiological changes and even age (with decreased enzymatic induction capacity)
should also be considered 1.

Nigrovic and Wierda have studied patients exposed
to succinylcholine and observed that smokers had a lower incidence of post-anesthetic
myalgia. The hypothesis was that nicotinic receptors would respond less vigorously
when stimulated by succinylcholine, which is a nicotinic agonist, but such findings
lack further confirmations 21.

ANESTHETIC MANAGEMENT OF SMOKING PATIENTS

COHb elimination half-life and patients physical
activities should be considered during pre-anesthetic evaluation. COHb elimination
half-life varies from 4 hours in a sedentary person to 1 hour in athletes. This
half-life is doubled during sleep. Smoking abstinence for 12 hours brings Hb
dissociation curve back to normal due to a decrease in COHb, increasing tissue
oxygenation. Even the blood of smoking donors has increased COHb levels, which
remain unchanged after 3 weeks of storage. Preoperative objectives are based
on secretions control, pulmonary function improvement and stopping smoking several
weeks before surgery (Chart
III) 1.

A risk level has been shown for cardiovascular
and respiratory systems. Currently, the passive smoking problem has been expanded
to possible anesthetic implications. Dennis et al. have shown that both active
and passive smokers suffer more adverse pulmonary events during anesthetic induction
than nonsmokers 26. Lyons et al. have shown that children exposed
to passive smoking suffer significantly higher postoperative oxygen desaturation
6,23.

Several studies have investigated preoperative
respiratory complications in smokers. Smokers have lower preoperative oxygen
arterial tension. Several studies suggest that they are more vulnerable to desaturation
after induction and sedation during anesthetic recovery, but other studies have
not confirmed such findings. This investigation is, in general, based on pulse
oximetry; few studies measure COHb values. Pulse oximetry responds to COHb as
if it were oxygenated Hb; so, oxygen saturation reported for smokers is probably
overestimated by several studies 3,6. Dennis et al., studying 120
patients ASA I and II, aged 18 to 75 years and submitted to elective surgeries
have concluded that during anesthetic induction, active and passive smokers
had a higher incidence of adverse effects as compared to nonsmokers. Those complications
were translated into high COHb concentrations and a higher number of Hb saturation
drops 26.

Caranza et al., in an experiment using nebulized
lidocaine before anesthetic induction, have observed a significant decrease
of procedure-related complications, indicating its use as part of previous management
of smoking patients 20.

Preanesthetic benzodiazepinic drugs may be used,
such as diazepam and midazolam. Parasympathomimetic agents, such as atropine,
glycopyrrolate and ipratropium seem to be useful. Glycopyrrolate is the drug
of choice for its long duration, lack of effects on the central nervous system
and minimum cardiovascular action 1.

Anesthetic Induction and Maintenance

In a study evaluating airway reflex sensitivity
to chemical and mechanical stimulations, Erskine et al. have observed its increase
in chronic smoking patients, which would determine a higher incidence of laryngospasms
and airway obstruction, with oxygen saturation decrease 27. A 24-hour
abstinence in a group of smokers has not produced significant changes but there
has been a progressive decrease in reflex sensitivity 24-48 hours after, with
consistent changes after 10 days. Other studies report a minimum 12-hour preoperative
abstinence, which would be enough to eliminate acute nicotine effects and, in
many cases, would decrease COHb to nonsmoker levels 3,6.

Short-term preoperative abstinence primarily
benefits the cardiovascular system; the respiratory system, however, needs at
least 6 weeks abstinence, according to Jones et al. 6. On the other
hand, Hill et al. evaluating heart surgery patients, have concluded that stopping
smoking for 8 weeks or longer determines postoperative pulmonary complication
levels similar to nonsmokers 14. A minimum 12-hour period could be
established as preoperative abstinence. Warner et al., in a prospective study
with patients submitted to coronary artery revascularization, have stressed
that 8 weeks are needed for morbidity to decrease to nonsmoker levels 6.

In inveterate smokers, the orientation to stop
smoking is more important. Stopping smoking is followed by secretions volume
and airway reactivity decrease, as well as by the increase in ciliary mucus
transportation. Such benefits, however, take 2 to 4 weeks to develop. Short-term
effects (48 to 72 hours) are associated to increased secretions and airway hyperactivity.
The only apparent advantage of stopping smoking in the immediate preoperative
period seems to be a decrease in COHb with a consequent tissue oxygenation improvement
18.

Some studies have observed acute upper airway
reflex response to larynx and lungs stimulation with cigarette smoke, but the
exact mechanism of this increased responsiveness caused by chronic exposure
to cigarettes is still not clear. Two mechanisms are considered to justify such
events: 1) acute pharmacological effects of the smoke on irritating receptors;
and 2) chronic changes in airway epithelium characteristics allowing the exposure
of irritating receptors located on the sub-epithelium to the chemical stimulation.
The first mechanism does not seem feasible since acute pharmacological effects
of nicotine or any other 4000 or more smoke components should disappear after
24-hours, which is opposed to the results of both studies performed by this
author. The second mechanism seems to be more consistent. Several studies have
suggested that airway epithelial layer damage or loss is a major factor to increase
their responsiveness, having also a role in restricting the access of inhaled
solutes to sub-epithelial structures. Chronic smokers develop laryngeal epithelium
inflammation, metaplasia and displasia and may break its integrity. In addition,
more recent data suggest that chronic smokers have decreased salivary epidermal
growth, which protects mucosa against acute injury helping in gastric healing
and duodenal ulcer prevention 27.

Postanesthetic Care and Complications

Historically, obesity and smoking are risk factors
for postoperative respiratory complications, since both are significant determinants
of severe pulmonary complications, as confirmed by Forrest et al. 2,28.
Obviously, the combination of obstructive ventilatory problems induced by smoking
and decreased functional residual capacity in obese patients leads to more severe
problems 2.

In general, postoperative pulmonary complications
are seen in 5% to 10% of surgical patients7; those submitted to abdominal
surgery have 4% to 22% of respiratory changes. Wong et al., in a study with
patients with severe chronic obstrutive pulmonary disease history, have observed
an increased long-term mortality when submitted to non-cardiac or chest surgeries
24. Severe DPOC patients exposed to non-chest surgeries had a long-term
mortality similar to those with severe coronary disease submitted to non-cardiac
surgery. This same author has concluded that patients with EFV1<
1.2L and submitted to non-cardiac or chest surgeries, had a 37% higher incidence
of postoperative pulmonary complications, excluding atelectasis, and 47% mortality
in two years. However, isolated preoperative pulmonary abnormalities are not
a prognosis for respiratory complications in patients with severe chronic obstrutive
pulmonary disease; in those cases, physical status (ASA) evaluation of respiratory
and non-respiratory factors should be considered.

Daley et al., studying hypoxemia-related changes
in patients admitted to PACU, have not associated previous smoking history to
such events 17. It is important to mention that patients with severe
pulmonary disease history were excluded from the study.

Long-term smokers should receive additional O2
during PACU transfer and be monitored by pulse oximetry or arterial blood gas
analysis. In some cases, there may be an increased need for analgesics due to
increased enzymatic induction 1.

Smokers are more dependent on cough to eliminate
tracheobronchic secretions. Secretion retention, as a result of the surgery
or the use of drugs, increase the possibility of airway obstruction and, as
a consequence, atelectasis. Patients should be encouraged to cough and take
deep breaths to eliminate tracheobronchic secretions. Physical therapy should
be considered in the immediate postoperative period 1.